Lymphogranuloma venereum is a sexually transmitted disease caused by serovars L1, L2 and L3 of Chlamydia trachomatis. During recent outbreaks, proctitis or proctocolitis predominated the clinical picture and the disease was mainly diagnosed in men who have sex with men.
The classic course of LGV consists of three stages that can be well distinguished. The incubation period may last up to one month, but symptom onset may also occur after a few days .
A primary lesion may form on vulva, vaginal mucosa or cervix, on the glans penis, most commonly on the coronal sulcus, in the urethra or rectum of both women and men. Depending on its precise location, it may go unnoticed unless mucopurulent discharge attracts the attention of the affected individual. It may appear as a papule or nodule, erode and ulcerate. If the latter is the case, hemorrhages may be reported. Contrary to lesions associated with genital herpes, pain and pruritus are generally absent. The primary lesion spontaneously remits after about one week.
The first stage of the disease is followed by a latency period of several weeks. The second stage of LGV is characterized by unilateral, rarely bilateral, lymphadenopathy; distinct lymph nodes may be affected dependent on the site of inoculation. In heterosexual men and some women, i.e., in those patients that presented the initial lesion in the anterior pubic area, inflammation of inguinal and external iliac lymph nodes occurs. In the developing world, this is the most common course of the disease, which is therefore often described as "genital ulcers and inguinal lymphadenopathy". Swelling and pain may be noted, but abscesses may also form in affected lymph nodes. They are commonly referred to as buboes, may rupture and drain into sinus tracts. In contrast, if inoculation occurs in the posterior pubic region, in the posterior parts of vulva and vagina, or in the rectum of women or men, pathogens may reach the perirectal and internal iliac lymph nodes. Here, lymphadenopathy provokes abdominal and lower back pain, but swollen lymph nodes are not palpable. Reactive arthritis has been reported to develop during the second stage of LGV .
If not adequately treated, the infection may persist for years and trigger a chronic inflammatory response. Extensive tissue damage, abscess and fistula formation, and, in case of anal infections, proctitis, strictures and stenosis of the rectum may occur during this third stage of LGV. Genital edema and lymphorrhoids are sometimes observed. These sequelae result from chronic lymphangitis, chronic edema and fibrotic remodelling processes.
Considering recent outbreaks in the developed world, presentation is more homogeneous. Most patients are homosexual or bisexual men and they usually suffer from hemorrhagic proctitis during early stages of the disease. This condition is painful and is often associated with anorectal bleedings and tenesmus.
If anamnestic data and clinical presentation prompt a suspicion of LVG, lesion or rectal swab specimens or aspirates from buboes should be obtained for further testing. Molecular biological approaches have been proven more reliable than traditional serological testing and bacterial culture. With regards to the latter, serological tests may be sensitive, but are rather unspecific, and culture of Chlamydia is a real challenge - it may be very specific, but is little sensitive.
Any approach chosen should be followed by genotyping, unless both steps can be realized in one single test. C. trachomatis is frequently detected in genital or rectal swabs, but L1, L2 or L3 serovars are rare findings. Because only those serovars are able to induce LGV, a definitive diagnosis cannot be made before genotyping results are available.
Due to the strong correlation between LGV and HIV infections, LGV patients should be tested for HIV infection. Similarly, diseases like hepatitis B, hepatitis C and syphilis are frequently observed in individuals pertaining to risk groups for LVG and thus, it should be ascertained if patients suffer from either of those infectious diseases.
Doxycycline is the antibiotic of choice to treat LGV, unless the drug is contraindicated - Pregnant and lactating women should rather be treated with azithromycin or erythromycin. In general, a therapeutic regimen of 100 mg doxycycline once a day per os for three weeks is recommended. Azithromycin is given in a single dose of 1 g per os; erythromycin needs to be applied for three weeks in daily doses of 500 mg. Antibiotic resistances have rarely been reported and if patients comply with prescriptions, relapses are unlikely. However, long-term protection cannot be conferred and if patients don't avoid risk behavior, renewed infection is to be expected.
If buboes are present, they should be drained. Proper wound care is also recommended.
LGV patients generally respond well to antibiotic treatment and their prognosis is very good if such therapy is initiated before extensive, irreversible tissue damage occurs.
LGV is a sexually transmitted disease caused by serovars L1, L2 and L3 of C. trachomatis. This Gram-negative pathogen pertains to the family of Chlamydiaceae and is known to cause a variety of other pathologies, some of which are transmitted during sexual intercourse. In detail, the latter applies for urethritis, cervicitis, epididymitis and prostatitis. However, these entities are provoked by distinct serovars and may neither result from nor lead to LGV.
LGV may be contracted during unprotected vaginal, anal or oral sex. These transmission routes are of different epidemiological importance: Vaginal sex is practiced by heterosexual individuals, and provokes LGV in women and men. It is the classical route of transmission. Anal sex has always accounted for minor shares of LGV cases, but has evolved to be the main way of transmission in recent outbreaks in Europe, North America and Australia. In agreement with that observation, the majority of patients in these countries are men who have sex with men. Oral LGV has only been reported anecdotally , and the importance of ano-oral transmission in recent outbreaks is not yet clear .
LGV has traditionally been considered a public health concern in developing countries. Here, low educational levels, lack of medical attention and commercial sex work contribute to an increase in incidence and prevalence among the respective risk groups. More recently, several outbreaks of LGV have been registered in industrialized nations. Affected individuals are generally men who have sex with man, particularly if presenting a concomitant infection with HIV. Of note, the latter scenario is not unknown in underdeveloped regions. Highest case numbers have been reported from the United Kingdom and France . And while the overall prevalence of LGV-associated serovars of C. trachomatis is much lower than that of other sexually transmitted strains  , almost one out of ten men who tested positive for C. trachomatis in the United Kingdom was indeed infected with an LGV-related serovar. Recent publications state that up to 25% of LGV patients remain asymptomatic; they may play an important role in epidemiology and serve as an undetected reservoir .
In general, women and men are equally susceptible to the disease. However, according to the above mentioned changes regarding risk groups and clinical presentation, males are diagnosed with LGV significantly more often than females in the Western world. With regards to age distribution, the sexually active population aged 15 to 40 years has a higher risk of contracting the disease than children and elder adults.
C. trachomatis is an obligate intracellular pathogen; it may be encountered in form of elementary bodies and reticulate bodies, which can be considered two developmental stages of the bacterium. Elementary bodies are infectious particles and may be transmitted during sexual intercourse. However, they are not metabolically active and require host cell structures in order to differentiate, grow and divide. Elementary bodies enter epithelial host cells within endocytic vacuoles after triggering cytoskeletal reorganization and induction of endocytosis . Inside the host cell, elementary bodies differentiate into reticulate bodies. These are metabolically active, grow, divide, and eventually re-differentiate into elementary bodies. Upon cell lysis, the latter are released and may infect other cells of the same host or be transmitted to another human being.
In contrast to other strains, serovars related with LVG frequently pass through the mucosal barrier, travel to regional lymph nodes via lymphatic vessels, infect monocytes and macrophages, and induce a lymphoproliferative reaction. Within weeks after infection, lymph node abscesses may form.
Practice of safer sex is a very effective way to prevent LVG and a plethora of other sexually transmitted diseases, and people should be adequately educated about this topic. If possible, condoms should be provided. However, these contraceptives may not in any case cover all LVG-associated lesions and thus, transmission cannot be ruled out even if condoms are used - a residual risk remains. Avoidance of sexual intercourse with people at high risk of LVG is strongly recommended and eventually the only way to further minimize the risk.
Frequent changes of sexual partners and commercial sex work predispose for an infection. In order to reduce morbidity and disease prevalence, every affected individual should be treated with antibiotics. Periodic screening of asymptomatic men that pertain to any of the above mentioned risk groups can be realized by examination of rectal swabs and may largely contribute to identify otherwise unnoticed reservoirs.
Lymphogranuloma venereum (LGV) is a sexually transmitted disease that has long since been considered a rare disorder in developed countries. However, case numbers have been rising during the last decade and LGV has recently been classified as a re-emerging infectious disease .
The etiologic agent of LGV is Chlamydia trachomatis (C. trachomatis), namely serovars L1, L2 and L3. The disease is endemic in underdeveloped regions of Africa, India, Southeast Asia, Central and South America. Here, it generally manifests in form of genital ulcers and inguinal lymphadenopathy. Although antibiotics are highly effective against the causative pathogen, appropriate medical attention is generally delayed or not at all available in the aforementioned regions. Thus, morbidity due to extensive tissue damage, abdominal pain and long-term sequelae is high.
In contrast, LGV is rarely diagnosed in industrialized nations of Europe and North America. However, an outbreak that occurred in the Netherlands in 2004 marked a turning point with regards to LGV epidemiology in the Western world: The disease has subsequently been observed in other European countries, in North America and in Australia. Highest incidence rates have been reported in the United Kingdom . Strikingly, the majority of these outbreaks has been provoked by serovar L2. Clinical presentation differed from the aforedescribed, classical one and was marked by complaints associated with proctitis or proctocolitis. Most patients were men who have sex with man, and a strong correlation between the incidence of LGV and previous infection with the human immunodeficiency virus (HIV) has been noted.
Lymphogranuloma venereum (LVG) is a sexually transmitted disease caused by serovars L1, L2 and L3 of Chlamydia trachomatis. It is important to note that other strains of this same species provoke distinct pathologies, i.e., inflammation of urethra, cervix, epididymis and prostate as well as conjunctivitis.
LVG may be contracted during unprotected vaginal, anal or - rarely - oral sex. Classic LVG manifests in form of genital or rectal ulcers and regional lymphadenopathy. Affected individuals pass through three stages of the disease: During the first stage, a papule may form on vulva, vaginal mucosa or cervix, on the glans penis, in the urethra or rectum of both women and men. It may erode and ulcerate, but is usually painless and doesn't cause pruritus. Thus, it frequently goes unnoticed. After about one week, it remits spontaneously. However, the infection persists, and symptoms corresponding to the second stage of the disease may be noted a few weeks later. By then, bacteria have reached regional lymph nodes, induce an inflammation accompanied by pain and swelling. Buboes may form. If not adequately treated, the disease may advance to a third, chronic stage marked by extensive tissue damage, abscess and fistula formation, and, in case of anal infections, inflammation, strictures and stenosis of the rectum.
While LVG has long since been considered an endemic disease of developing countries, several outbreaks have been registered in recent years in Europe, North America and Australia. The vast majority of affected individuals were men who have sex with man, whereby many of them were also infected with the human immunodeficiency virus. In these cases, an inflammation of the rectum or rectum and colon predominated the clinical picture. Patients may not anorectal bleedings, hemopurulent discharge, and problems while defecating.
LVG is effectively treated with antibiotics. If therapy is initiated before irreversible tissue damage occurs, the prognosis is excellent and long-term sequelae are not to be expected.